Sepsis is defined as an organ dysfunction which compromise one’s life resulted from a dysregulated response to infection [1]. Sepsis is a common clinical emergency based on statistics, over 53,000 folks die annually due to sepsis, the total mortality rate is evaluated to be nearly one-third [1], [2], [3]. As a significant mediator of inflammation, Interleukin 6 (IL-6) is released by lymphocytes, monocytes/macrophages. It promotes the release of other inflammatory factors in large quantities, triggers an inflammatory waterfall-like response, and is closely associated with the inflammatory immune system response and severe systemic infections, and both in transcription and post-transcription its expression is strictly controlled [4], [5], [6]. Single nucleotide polymorphisms (SNPs), in genomic association studies, is the most ordinary variation of genes, in which promoters may have a function in regulating transcriptional expression [7]. The human IL-6 gene is responsible for regulating transcriptional activity during the inflammatory response, and its −572 G/C serves as one of the hotspots SNPs, which may influence IL-6 transcriptional activity [4], [5], [6], [8]. Indeed, some studies [9], [10] have suggested the correlation between the polymorphisms of IL-6-572G/C and various inflammatory diseases, which may provide new ideas for the diagnosis and treatment of sepsis. A meta-analysis study suggested that no remarkable association between the development of sepsis and the IL-6-572G/C polymorphism was found [11]. Therefore, promoter region of IL-6 gene polymorphisms's relativity with sepsis still needs to be explored, and this study provides theoretical guidance for the clinical diagnosis, prevention, and treatment of sepsis by comprehensively evaluating RCTs investigating the relevancy in the polymorphism of IL-6-572G/C polymorphism and sepsis.